Relevant bibliographies by topics / Circulating Leukocytes

Academic literature on the topic 'Circulating Leukocytes'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Circulating Leukocytes"

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AKHUND, ISRAR AHMED, IRSHAD ALI ALVI, GHULAM RASOOL BHURGRI, Muhammad Ali Qureshi, and Haji Khan Khoharo. "CIRCULATING LEUKOCYTES." Professional Medical Journal 17, no. 03 (September 10, 2010): 455–58. http://dx.doi.org/10.29309/tpmj/2010.17.03.2804.

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Objective: Evaluating circulating leukocytes in acute mental stress & relation with coronary artery disease. Design: Descriptive study Setting: Muhammad Medical College Mirpurkhas, Duration: from March 2007 to August 2007. Methods: Two hundred young healthy adults were studied for stress experiment. Venous blood samples were drawn before and after stress for estimation of leukocyte counts. Values were presented as mean ±standard error of mean (SEM). Results: The difference in Pre and during stress results of variables were TLC = - 4630.85 ± 140.65, N % = -11.8 ± 0.36, L% = 4.03 ± 0.14, M %= 5.48 ± 0.37, E % = 1.18 ± 0.07, B % = 1.11 ± 0.022. Highly significant p-values (≤ 0.001) were found among various parameters, in both groups of subjects. Conclusion: An increase in the number of circulating leukocytes was an important unexpected observation that was noted. We suggest that the real life stress induced leukocytes changes may warrant further investigation about its relation with the coronary artery disease (CAD).
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Kirchhofer, Daniel, Markus A. Riederer, and Hans R. Baumgartner. "Specific Accumulation of Circulating Monocytes and Polymorphonuclear Leukocytes on Platelet Thrombi in a Vascular Injury Model." Blood 89, no. 4 (February 15, 1997): 1270–78. http://dx.doi.org/10.1182/blood.v89.4.1270.

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AbstractThe adhesion of leukocytes to platelets deposited at the site of vascular injury may represent an important mechanism by which leukocytes contribute to hemostasis and thrombosis. In this study, we examined whether, in comparison with their distribution in circulating blood, certain leukocyte types are enriched at sites of platelet deposition. We used an experimental vascular injury model, in which human fibrillar collagen was exposed to anticoagulated human whole blood flowing through parallel-plate chambers (venous shear rate, 65/s). The platelet-adherent leukocytes were detached by EDTA treatment and analyzed by flow cytometry using cell-type–specific antibodies. The predominant leukocytes found in platelet thrombi were polymorphonuclear leukocytes, accounting for 76% of bound leukocytes (62% in circulating blood), whereas T and B lymphocytes did not significantly accumulate on thrombi, comprising a fraction of less than 5% (32% in circulating blood). Monocytes constituted 16% of platelet thrombus-bound leukocytes, which represents an almost fourfold enrichment as compared with their proportion in circulating blood. Almost identical results were obtained when we analyzed leukocytes adhering to platelet monolayers, which were formed by blocking glycoprotein IIb-IIIa, thus preventing platelet aggregation on top of the collagen-adherent platelets. Furthermore, leukocyte adhesion to platelet monolayers was completely inhibited by an anti-P-selectin antibody (50% inhibitory concentration, 0.3 μg/mL), whereas it reached a plateau at about 70% inhibition on platelet thrombi. This difference could be explained by a possible function of glycoprotein IIb-IIIa in leukocyte immobilization to thrombi or by the high local concentration of P-selectin in the growing thrombi. The results suggest that, because of their known abilities to promote coagulation and thrombolysis, the monocytes and polymorphonuclear leukocytes accumulating on forming platelet thrombi could play an important role in modulating thrombotic and hemostatic processes.
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Donahue, Robert E., Laura Tuschong, Thomas R. Bauer, Yu Ying Yau, Susan F. Leitman, and Dennis D. Hickstein. "Leukocyte integrin activation mediates transient neutropenia after G-CSF administration." Blood 118, no. 15 (October 13, 2011): 4209–14. http://dx.doi.org/10.1182/blood-2011-06-360461.

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Abstract After administration of granulocyte colony-stimulating factor (G-CSF), there is a marked, albeit transient, drop in circulating neutrophils. To determine the role of leukocyte integrins in this disappearance, a dog having canine leukocyte adhesion deficiency (CLAD) or CLAD dogs who had undergone gene correction either by matched littermate allogeneic transplant or autologous gene therapy were evaluated. Shortly after G-CSF administration, a dramatic, yet transient, neutropenia was observed in the control littermates. This neutropenia was not as marked in the CLAD dogs. In all instances, it was CD18+ neutrophils that preferentially egressed from the circulation. The association of CD18 with this rapid loss suggested leukocyte integrin activation after G-CSF administration. To determine the activation status of the integrin, a monoclonal antibody recognizing the activated α-subunit cation binding domain (mAb24) was used to evaluate human leukocytes after G-CSF administration. Mirroring the dramatic decrease in circulating neutrophil numbers, there was a dramatic and specific increase in the activation of the α-subunit after G-CSF expression on polymorphonuclear leukocytes. This activation, like the drop in neutrophil count, was transient. These results demonstrate that the leukocyte integrin on circulating neutrophils is transiently activated after G-CSF administration and mediates the transient neutropenia observed after G-CSF administration.
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Wang, Yongzhi, Jonas Roller, Jan E. Slotta, Su Zhang, Lingtao Luo, Milladur Rahman, Ingvar Syk, Michael D. Menger, and Henrik Thorlacius. "Distinct patterns of leukocyte recruitment in the pulmonary microvasculature in response to local and systemic inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 4 (February 15, 2013): L298—L305. http://dx.doi.org/10.1152/ajplung.00246.2012.

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The mechanisms of leukocyte recruitment in the pulmonary microvasculature in response to local and systemic inflammation remain elusive. Male C57BL/6 mice received lipopolysaccharide (LPS) intrapulmonary (intratracheally, it) or systemically (intravenously, iv) for 1–18 h. Leukocyte responses in lung were analyzed by use of intravital fluorescence microscopy. Plasma and lung levels of CXC chemokines as well as Mac-1 and F-actin expression in leukocytes and bronchoalveolar leukocytes were quantified. Venular leukocyte rolling was markedly increased in response to local LPS but only marginally after systemic LPS. Leukocyte adhesion in venules was enhanced in both groups although adhesion was higher in mice receiving LPS intratracheally compared with LPS intravenously. Systemic LPS caused more leukocytes trapping in capillaries compared with local LPS. The ratio of adherent leukocytes in venules compared with capillaries was higher in response to local LPS, suggesting that leukocytes were more prone to accumulate in venules in local inflammation and in capillaries in systemic inflammation. Systemic LPS triggered higher F-actin formation and Mac-1 expression in leukocytes compared with local LPS. Local and systemic LPS caused similar increases in CXC chemokines in the lung whereas intravenous endotoxin provoked higher levels of CXC chemokines in the circulation. Interestingly, intratracheal LPS increased recruitment of leukocytes in the alveolar space whereas intravenous LPS was ineffective in promoting leukocyte accumulation in the bronchoalveolar space. In conclusion, our data demonstrate that pulmonary microvascular recruitment of leukocytes differs in local and systemic inflammation, which might be related to premature activation and stiffening of circulating leukocytes in endotoxemia.
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Tjwa, Marc, Lola Bellido-Martin, Yuan Lin, Esther Lutgens, Stéphane Plaisance, Françoise Bono, Nathalie Delesque-Touchard, et al. "Gas6 promotes inflammation by enhancing interactions between endothelial cells, platelets, and leukocytes." Blood 111, no. 8 (April 15, 2008): 4096–105. http://dx.doi.org/10.1182/blood-2007-05-089565.

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AbstractThe role of Gas6 in endothelial cell (EC) function remains incompletely characterized. Here we report that Gas6 amplifies EC activation in response to inflammatory stimuli in vitro. In vivo, Gas6 promotes and accelerates the sequestration of circulating platelets and leukocytes on activated endothelium as well as the formation and endothelial sequestration of circulating platelet-leukocyte conjugates. In addition, Gas6 promotes leukocyte extravasation, inflammation, and thrombosis in mouse models of inflammation (endotoxinemia, vasculitis, heart transplantation). Thus, Gas6 amplifies EC activation, thereby playing a key role in enhancing the interactions between ECs, platelets, and leukocytes during inflammation.
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Teraoka, S., M. Sugawara, Y. Kitano, T. Hoshino, M. Takahashi, Y. Minagawa, S. Naganuma, et al. "Microscopic Observation of Leukocyte Kinesis in the Vascular Bed during Hemodialysis Using the Rabbit Ear Chamber Technique." International Journal of Artificial Organs 12, no. 4 (April 1989): 229–33. http://dx.doi.org/10.1177/039139888901200405.

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Leukocyte kinesis in the capillary vascular bed during hemodialysis (HD) was investigated to elucidate the mechanism of transient leukopenia. Leukocyte movement was observed microscopically during HD using the rabbit ear chamber (REC) technique, which permits visualization of the movement of blood corpuscles in capillaries. Blood was drawn from the femoral artery and returned into the auricular and/or carotid artery so that the blood passing through the hollow fiber artificial kidney (HFAK) flowed into capillaries in the REC. Leukocyte counts of blood samples taken from the afferent and efferent limbs of the HD circuit, the right jugular vein and the right atrium were determined consecutively during HD. The difference in the leukocyte count was observed between the afferent and efferent limbs for the first 15 minutes and thereafter between the efferent limb and the jugular vein. The “transpulmonary” difference in the leukocyte count was not noticed throughout HD. Between 15 and 90 minutes after the start of HD, scarcely any circulating leukocytes were found in capillaries in the REC and some leukocytes were attached to the endothelial surface. Thereafter circulating leukocytes were seen again and detachment of leukocytes from the endothelial surface was observed. No leukocyte aggregation or embolization of aggregating leukocytes was noticed. This evidence suggests that leukopenia may be attributed to the transient shift of leukocytes to the marginal pool of the vessel lumen and this process may not be specific for the pulmonary vasculature, but may occur in the first capillary bed into which the blood passing through the HFAK flows. The attachment of leukocytes to the surface membrane of the HFAK may contribute to the transient leukopenia especially during the initial period of the HD.
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Pistiki, Aikaterini, Anuradha Ramoji, Oleg Ryabchykov, Daniel Thomas-Rüddel, Adrian T. Press, Oliwia Makarewicz, Evangelos J. Giamarellos-Bourboulis, et al. "Biochemical Analysis of Leukocytes after In Vitro and In Vivo Activation with Bacterial and Fungal Pathogens Using Raman Spectroscopy." International Journal of Molecular Sciences 22, no. 19 (September 28, 2021): 10481. http://dx.doi.org/10.3390/ijms221910481.

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Biochemical information from activated leukocytes provide valuable diagnostic information. In this study, Raman spectroscopy was applied as a label-free analytical technique to characterize the activation pattern of leukocyte subpopulations in an in vitro infection model. Neutrophils, monocytes, and lymphocytes were isolated from healthy volunteers and stimulated with heat-inactivated clinical isolates of Candida albicans, Staphylococcus aureus, and Klebsiella pneumoniae. Binary classification models could identify the presence of infection for monocytes and lymphocytes, classify the type of infection as bacterial or fungal for neutrophils, monocytes, and lymphocytes and distinguish the cause of infection as Gram-negative or Gram-positive bacteria in the monocyte subpopulation. Changes in single-cell Raman spectra, upon leukocyte stimulation, can be explained with biochemical changes due to the leukocyte’s specific reaction to each type of pathogen. Raman spectra of leukocytes from the in vitro infection model were compared with spectra from leukocytes of patients with infection (DRKS-ID: DRKS00006265) with the same pathogen groups, and a good agreement was revealed. Our study elucidates the potential of Raman spectroscopy-based single-cell analysis for the differentiation of circulating leukocyte subtypes and identification of the infection by probing the molecular phenotype of those cells.
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Li, Nailin, Anne Soop, Alf Sollevi, and Paul Hjemdahl. "Multi-Cellular Activation In Vivo by Endotoxin in Humans – Limited Protection by Adenosine Infusion." Thrombosis and Haemostasis 84, no. 09 (2000): 381–87. http://dx.doi.org/10.1055/s-0037-1614032.

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SummaryThe influence of adenosine infusion (40 µg/kg/min for 4 h) on inflammatory and hemostatic parameters was investigated in healthy males without (n = 10) or with (n = 11) intravenous endotoxin injection (4 ng/kg). Without endotoxin, adenosine elevated circulating leukocytes and circulating platelet-leukocyte aggregates. Endotoxin activated platelets and leukocytes in vivo. Platelet activation was seen as slightly increased platelet P-selectin expression, decreased platelet counts, and elevated plasma soluble P-selectin (from 39.6 ± 3.4 to 68.9 ± 6.6 ng/ml; P <0.01). Leukocyte activation was evidenced by increased CD11b expression (from MFI of 0.54 ± 0.02 to 2.21 ± 0.17; P <0.01) and plasma elastase levels (from 25.3 ± 2.5 to 169.3 ± 22.5 ng/ml; P <0.01). Endotoxin also enhanced platelet and leukocyte responsiveness to in vitro stimulation. Endotoxin induced von Willebrand factor secretion (from 92 ± 8 units to 265 ± 19 units at 4 h; P <0.001) and enhanced thrombin generation in vivo. Endotoxin induced leukocytosis and thus increased circulating platelet-leukocyte, mainly platelet-neutrophil, aggregates. Adenosine caused slight attenuation of platelet reactivity to agonist stimulation, enhanced the endotoxin-induced leukocytosis, and detained more platelet-leukocyte aggregates in circulation, but did not attenuate endotoxin-induced neutrophil elastase secretion, von Willebrand factor secretion, or thrombin generation. Thus, endotoxemia induces multi-cellular activation in vivo. Adenosine inhibits leukocyte adhesion and extravasation, and mildly attenuates platelet responsiveness and soluble P-selectin release. Adenosine has the potential of becoming a therapeutic antiinflammatory drug, but an optimal treatment strategy needs to be developed.
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Almeida, Camila Bononi, Maria Emilia Favero, Fernanda Gonçalves Pereira-Cunha, Irene Lorand-Metze, Sara T. Olalla Saad, Fernando Ferreira Costa, and Nicola Conran. "Alterations in cell maturity and serum survival factors may modulate neutrophil numbers in sickle cell disease." Experimental Biology and Medicine 236, no. 11 (November 2011): 1239–46. http://dx.doi.org/10.1258/ebm.2011.011130.

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Leukocytes are known to exacerbate inflammatory and vaso-occlusive processes in sickle cell disease (SCD). The aim of this study was to determine whether alterations in neutrophil maturity and/or cell-death modulating factors in the circulation contribute to the increased leukocyte counts and leukocyte survival observed in SCD. The maturity of circulating neutrophils from healthy control individuals (CON), SCD and SCD patients on hydroxyurea therapy (SCDHU) was determined immunophenotypically. Serum factors affecting neutrophil apoptosis (determined by annexin V-binding) were analyzed by culturing control neutrophils (CON neutrophils) with pooled serum from CON, SCD and SCDHU individuals. Immunophenotypic characterization of neutrophils suggested a slight, but significant, increase in the circulation of immature neutrophils in SCD. While SCD neutrophils cultured in the presence of CON serum presented delayed apoptosis, unexpectedly, the culture of CON neutrophils with SCD serum significantly augmented apoptosis and caspase-9 activity. Inhibition of the activity of serum interleukin-8, a neutrophil-apoptosis-inhibiting cytokine, significantly increased SCD serum-induced CON neutrophil apoptosis, indicating that SCD serum may have both apoptotic and antiapoptotic properties. The decreased maturity of SCD neutrophils observed is suggestive of an accelerated immigration of leukocytes from the bone marrow to the circulating pool that may contribute to an increase in cell survival, subject to modulation by a complex balance of both anti- and proapoptotic factors contained in the circulation of SCD individuals.
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Gào, Xīn, Yan Zhang, Xiangwei Li, Lina Jansen, Elizabeth Alwers, Melanie Bewerunge-Hudler, Matthias Schick, Jenny Chang-Claude, Michael Hoffmeister, and Hermann Brenner. "DNA Methylation-Based Estimates of Circulating Leukocyte Composition for Predicting Colorectal Cancer Survival: A Prospective Cohort Study." Cancers 13, no. 12 (June 12, 2021): 2948. http://dx.doi.org/10.3390/cancers13122948.

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Leukocytes are involved in the progression of colorectal cancer (CRC). The proportion of six major leukocyte subtypes can be estimated using epigenome-wide DNA methylation (DNAm) data from stored blood samples. Whether the composition of circulating leukocytes can be used as a prognostic factor is unclear. DNAm-based leukocyte proportions were obtained from a prospective cohort of 2206 CRC patients. Multivariate Cox regression models and survival curves were applied to assess associations between leukocyte composition and survival outcomes. A higher proportion of lymphocytes, including CD4+ T cells, CD8+ T cells, B cells, and NK cells, was associated with better survival, while a higher proportion of neutrophils was associated with poorer survival. CD4+ T cells outperformed other leukocytes in estimating the patients’ prognosis. Comparing the highest quantile to the lowest quantile of CD4+ T cells, hazard ratios (95% confidence intervals) of all-cause and CRC-specific mortality were 0.59 (0.48, 0.72) and 0.59 (0.45, 0.77), respectively. Furthermore, the association of CD4+ T cells and prognosis was stronger among patients with early or intermediate CRC or patients with colon cancer. In conclusion, the composition of circulating leukocytes estimated from DNAm, particularly the proportions of CD4+ T cells, could be used as promising independent predictors of CRC survival.
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Dissertations / Theses on the topic "Circulating Leukocytes"

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Klimecki, Walter Thomas. "P-glycoprotein: Expression and function in normal circulating leukocytes." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186715.

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P-glycoprotein (P-gly) is a well characterized membrane protein, expressed in cancer cells, functioning as an efflux pump. This function confers drug-resistance. P-gly is also expressed in normal tissues such as the liver and kidney. In normal tissues P-gly has restricted expression. In the kidney P-gly is expressed in tubular brush border. This suggests a physiologic role for P-gly. A goal of this work was to determine whether P-gly, if present in leukocytes, followed the cell-type restriction seen in other P-gly positive normal tissues. Assays measuring P-gly included immunofluorescence, immunocytochemistry, and immunoblot analysis. Northern blot analysis and RT-PCR were used to measure mdr1 mRNA. P-gly function was assayed by measuring the verapamil-sensitive retention of rhodamine 123 (rh123). Immunofluorescent staining of leukocytes for lineage and P-gly revealed high levels of P-gly in CD56+ cells. CD8+ cells followed in staining, with CD4+ and CD19+ cells at intermediate levels, and CD14+ and CD15+ cells staining at background. RNA analysis by RT-PCR confirmed the immunofluorescence data, except for CD15+ cells, which demonstrated mdr1 mRNA similar to CD4+ cells. Function assays confirmed the immunofluorescence results, with efficient clearing of dye from CD56+ cells, followed by CD8+, CD4+, and CD19+ cells. CD14+ and CD15+ cells did not demonstrate P-gly function. Immunoblot analysis of membranes and immunocytochemical analysis of CD15+ cells demonstrated P-gly. The high level of functional P-gly observed in CD56+ cells prompted experiments to determine whether P-gly was involved in the CD56+ mediated cytolytic response. Using 4 inhibitors of P-gly mediated efflux, cyclosporine A, PSC 833, R-verapamil, and S-verapamil, NK cells were assayed for cytolytic function. Each compound demonstrated dose-response relationships in inhibiting NK-mediated cytolysis. Each compound also demonstrated a dose-response in inhibition of P-gly mediated efflux, although there was not an exact correlation between efflux inhibition and cytolysis inhibition. Nevertheless, the data in this study demonstrate a relatively high level of P-gly expression in CD56+ and CD8+ cells. In addition, the data support a role for P-gly in the cytolytic function of NK cells, although the point of P-gly involvement in the process of cytolysis remains to be defined.
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Herwanto, Velma. "IMMUNOMETABOLISM OF CIRCULATING LEUKOCYTES IN PATIENTS WITH INFECTION AND SEPSIS." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24414.

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Immune dysfunction is a major complication of sepsis. It increases susceptibility to nosocomial infection and contributes significantly to sepsis mortality. Immune dysfunction in sepsis has been associated with alterations in cellular metabolism which manifest as mitochondrial dysfunction and reduced cellular energy production. However, those alterations have been shown in established sepsis patients. Data are lacking in patients who are at early phase of infection who are yet to progress to sepsis. Our study aims to address this knowledge gap. Here, we present findings of a study that investigates metabolic alterations in the immune cells of infection patients. In particular, we compare the findings between those who develop sepsis with findings in those who did not develop sepsis (uncomplicated infection patients) to identify key pathologic mechanisms that underlie the progression from uncomplicated infection towards complicated infection (that is, sepsis). First, in an in vitro model of sepsis, our preliminary experiment on peripheral blood mononuclear cells (PBMCs) indicated reduced mitochondrial respiration with increased intramitochondrial oxidative stress. Second, impaired mitochondrial respiration, with increased intramitochondrial oxidative stress, was observed in the PBMCs of patients with sepsis recruited from the emergency department. The level of oxidative stress significantly correlated with the severity of mitochondrial respiration impairment. Third, the findings of impaired mitochondrial respiration and increased intramitochondrial oxidative stress were also observed in patients with uncomplicated infection, albeit to a lesser intensity. Lastly, further study on the PBMCs subsets, monocyte and T lymphocytes, corroborated the findings of metabolic alterations in sepsis as well as in uncomplicated infection patients. Altogether, our study found that impaired mitochondrial respiration is detected in the immune cells of patients with uncomplicated infection, as it is in sepsis. Intramitochondrial oxidative stress is among several factors inducing the mitochondrial impairment, raising a possibility of its role as a potential target for preventing immune dysfunction.
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Melki, Vilyam. "Nitric oxide : An ally in extracorporeal circulation?" Doctoral thesis, Uppsala universitet, Thoraxkirurgi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-298782.

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Many complications associated with heart surgery are due to the negative effects of extracorporeal circulation (ECC). Some of these complications may be attributed to ECC-induced activation of inflammation and coagulation pathways. The inflammatory reaction may be caused by the interaction of blood components with air and the artificial surfaces of the ECC, from substances produced due to ischaemia-reperfusion injury of the heart and lungs, and from increased release of endotoxin from ischemic intestines. Staphylococcus aureus (S. aureus) infections are the leading cause of respiratory, skin and soft tissue, and bloodstream infections. Nitric oxide (NO) is a gaseous signaling molecule involved in many physiological and pathological processes. The role of NO in infection and inflammation is complex. NO may contribute to morbidity by acting as a vasodilator, myocardial depressant, and cytotoxic mediator. On the other hand, NO may have a salutary role through microvascular, cytoprotective, immunoregulatory, and antimicrobial properties. A simulated extracorporeal circulation (SECC) model is a closed circuit, including a roller pump, an oxygenator, a venous reservoir and polyvinyl chloride (PVC) tubing, where human blood is circulated. The SECC model allows studies of the blood and its components, without any influence from other organ systems. The aim of this work was to investigate NO effects during SECC and in S. aureus infection. Study I. Human blood was circulated through SECC during 3 hours, and leukocyte granule release was studied. Results indicated that NO addition during SECC is pro-inflammatory by stimulating leukocyte activation and granule release, and has no effect on oxygen free radical production and interleukin release. Study II. Investigating the effect of NO on S. aureus growth in whole blood during 180 min SECC, results showed a 6.2 fold growth in the presence of NO. Results indicated that by stimulating the expression of inducible lactate dehydrogenase, specific to S. aureus, NO may improve S. aureus resistance to oxidative stress, giving the pathogen a survival advantage. Study III. In an in vitro system of SECC, we measured glyceryl trinitrate (GTN) induced changes in leukocyte activation in whole blood caused by S. aureus infestation, as well as the effect of GTN on S. aureus growth. Results indicated that GTN does not affect S. aureus growth during SECC and has no effect on SECC-induced leukocyte activation. Study IV. Whole blood concentrations of selected leukocyte adhesion molecules, complement system components and myeloperoxidase  were measured in an in vitro system of SECC. Results indicated that SECC induces the increased expression of some leukocyte markers and that GTN addition significantly reduces the expression of some leukocyte activation markers.
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Hergenhan, Sophia Martina [Verfasser], and Christoph [Akademischer Betreuer] Scheiermann. "Circadian control of leukocyte numbers in the circulation / Sophia Martina Hergenhan ; Betreuer: Christoph Scheiermann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1211957373/34.

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Wu, Xianai. "Deoxynivalenol alters circulating and splenic leukocyte and cell migration markers in interaction with time course and sex in young and old BALB /c mice." [Ames, Iowa : Iowa State University], 2008.

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Tomić, Lidija. "Studies on Retinal Circulation in Experimental Animals, Healthy Human Eyes and Eyes with Diabetic Retinopathy." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9396.

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The retina is a highly metabolically active tissue with large demands on the supply of nutrients. Disorders affecting the retina often include some vasculopathy with an impact on retinal circulation. Studies of retinal haemodynamics could thus help to detect, differentiate and diagnose diseases, to monitor changes in disease as well as progression and efficiency of the therapy. The present studies were an attempt to validate and determine the clinical usefulness of a newly developed technique for studying the retinal circulation in human eyes. We used different techniques to evaluate different parameters of retinal circulation. We examined how leukocyte velocity determined with Blue Field Simulation and transit times, mean transite time (MTT) and arterio-venous passage (AVP), and vessel diameter, determined from fluorescein angiograms, together reflects the retinal circulation. MTT was determined with a method based on an Impulse-Response technique, MTTIR. In a study on monkeys we compared our method, together with two conventional methods, with an absolute measurement of retinal blood flow (RBF) determined with labelled microspheres. There was a weak, but not statistically significant, correlation between retinal blood flow and MTTIR (r2 = -0.60, p = 0.06), but no useful correlation between retinal blood flow and either of the other two measures of transit times. In a study on healthy eyes we determined the effect of a physiological provocation, changes in arterial blood gases, on retinal circulation. Breathing pure oxygen or increased level of carbon dioxide in inspired air had no effect on MTT, but oxygen reduced leukocyte velocity and vessel diameter and carbon dioxide increased leukocyte velocity significantly. We concluded that unchanged transit time trough the retinal tissue was not due to a lack of effect of the gas provocation but a result due to concomitant changes in volume and flow. In a study on eyes of patients with diabetic retinopathy we investigated the relation between the extent of retinal circulation changes and the severity of the diabetes retinopathy (DRP). Transit times were relatively unaffected until proliferative DRP (PDRP) developed. In eyes with PDRP both MTTIR and AVP were increased. After panretinal photocoagulation treatment MTTIR returned to normal levels and vessel diameters tended to decrease while leukocyte velocity and AVP remained unchanged. We concluded that the increase in MTTIR in eyes with PDRP is at least partly explained by vessel dilation, causing an increased volume of the retinal vascular bed.
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Troianova. "HIGH-THROUGHPUT CHARACTERIZATION OF CIRCULATING LEUKOCYTE ALTERATIONS IN MALE AND FEMALE COPD PATIENTS." Doctoral thesis, 2021. http://hdl.handle.net/11562/1048691.

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Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Nowadays, COPD is the fourth leading cause of death in the world and its morbidity and mortality are constantly increasing. COPD is characterized by emphysema and chronic bronchitis, usually present simultaneously, with a wide range of severity. COPD was considered as a lung-restricted disease for many years, but from 2000 increasing new evidence, including a number of comorbid conditions accompanying this pathology and the presence of systemic inflammation, indicate that COPD should be considered a systemic disease. Systemic inflammation is the most common systemic manifestation of COPD, and it is associated with a progressive worsening of symptoms and comorbidities. In addition to soluble inflammatory markers, such as TNFα, several research groups focused their attention on peripheral blood leukocytes to assess the changes occurring in these cells in COPD and their relation to the inflammatory pattern in the lungs. However, the data about peripheral leukocyte composition and functional changes in COPD are quite controversial. COPD was traditionally considered as a disease affecting principally males, but rising evidence show that it probably equally concerns male and female populations. However, there are differences in symptoms severity, disease progression and treatment benefits between male and female COPD. Yet, despite the clear evidence of sexual dimorphism in COPD manifestation and progression, there are, to our knowledge, no publications about the difference in the immune state between male and female COPD. Given the lack of data assessing gender-related differences in COPD systemic immune system manifestations and the discordance in the data about circulating leukocyte alterations in COPD, we aimed at thoroughly characterize circulating leukocyte alterations in COPD as compared to age-matched controls. Additionally, results have been stratified according to gender in order to identify male- and/or female-specific COPD immunophenotype. Blood samples from 50 COPD patients and 63 age and sex-matched controls have been collected and analyzed. Flow cytometry analysis revealed the existence of well-defined gender-related pattern of circulating leukocytes in COPD. Specifically, while neutrophilia and increased neutrophil to lymphocyte ratio are hallmarks of COPD in male, on the contrary, female COPD are characterized by a generalized leukopenia. Remarkably, we demonstrated that T cell exhaustion is more prominent in female COPD, nevertheless it increases with disease severity in both male and female groups. Moreover, several observations suggest that that T cells decrease in both male and female COPD may be related to PD1-dependent apoptosis. Additionally, we showed that absolute numbers and/or frequencies of several leukocyte populations correlate with different clinical parameters of COPD disease severity. Given the relevance of the increase in neutrophil absolute count and frequency in male COPD, we subsequently characterized circulating neutrophil phenotype, function and transcriptome of male COPD and related controls. Despite the fact that phenotype and function of neutrophils purified from COPD subjects were comparable to those from controls, differential gene expression analysis highlighted a number of differentially expressed genes. On the basis of the correlation of the differentially expressed genes with the disease severity, we identified a neutrophil-specific COPD signature. Finally, this proposed COPD signature was successfully validated on a larger cohort of male COPD subjects.
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Rautenbach, Hanli. "A study on the effect of a complex formula consisting of homoeopathic Thuja occidentalis DI and Baptisia tinctoria mother tincture on circulating leukocytes." Thesis, 2014. http://hdl.handle.net/10210/11492.

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M.Tech. (Homoeopathy)
Baptisia tinctoria and Thuja occidentalis are reported to be immunostimulants, and thus have an effect on white blood cells. Little formal research has been done to demonstrate their effects on the different white cell populations. The purpose of this study was to determine the effects of these substances on the circulating leukocytes, and to compare these effects to a placebo. An initial full blood count was conducted to establish a baseline level for each subject. The subjects were required to take 18.75 millilitres of the medication or placebo in split doses over a three-hour period. Thereafter, a second full blood count was taken at one-hour intervals. The medication appeared to cause an increase in the lymphocyte count, thus suggesting a possible indication for viral infection. There was an increase in both groups of the total WBC count as well as in the lymphocyte count, raising the question of what substance actually caused these changes to occur. Expansion of this study, including using a larger sample size and longer test period, may be required to validate these results.
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Scarcella, Daniela. "A study on the effect of a homoeopathic complex formula consisting of Baptisia tinctoria mother tincture and Echinacea purpurea mother tincture on circulating leukocytes." Thesis, 2014. http://hdl.handle.net/10210/11779.

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Davey, Karen Lee. "A study on the effect of a homoeopathic complex formula consisting of Echinacea purpurea tincture, Echinacea angustifolia tincture, Bapstisia tinctoria tincture and Thuja occidentalis D1 on circulating leukocytes." Thesis, 2014. http://hdl.handle.net/10210/9043.

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M.Tech. (Homoeopathy)
The purpose of this study is to determine the effect of the homoeopathic complex formula consisting of , Echinacea angustifolia tincture, Baptisia tinctoria tincture and Thuja occidentalis D1 on circulating leukocytes. These medicinal plants have immune enhancing properties and an effect on leukocytes. Leukocytes play an important role in the body's defence system. 54 volunteers participated in a randomised double blind placebo controlled trial. An initial full blood count before treatment served as a base-line control for each volunteer. A total of 15ml of the medication placebo was administered over 3 hours. After the last dose, a further three blood samples were drawn at 90 minute intervals. Blood analysis included a differential leukocyte count. The trial was conducted over a single 6 hour period. The homoeopathic medication caused a decrease in circulating leukocytes, specifically lymphocytes. The efficacy of this medicationas an immunostimulant should be confirmed on a larger study sample.
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Books on the topic "Circulating Leukocytes"

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Tay, Tuan Leng, Giuseppe Locatelli, Gabriela Constantin, and V. Wee Yong, eds. Understanding the Roles of Glia and Circulating Leukocytes in Neurodegenerative Diseases. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-070-1.

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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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Book chapters on the topic "Circulating Leukocytes"

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Bryant, Amy E., and Dennis L. Stevens. "Expression of Activational Markers on Circulating Leukocytes from Baboons with Group A Streptococcal (GAS) Bacteremia." In Streptococci and the Host, 801–4. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_189.

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Gabriele, S., A. M. Benoliel, P. Bongrand, and O. Theodoly. "Microfluidic Modeling of Circulating Leukocyte Deformation." In IFMBE Proceedings, 1959–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89208-3_467.

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Mage, Rose G., and Claire Rogel-Gaillard. "Immunogenetics in the rabbit." In The genetics and genomics of the rabbit, 66–83. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781780643342.0005.

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Abstract This chapter on immunogenetics in the rabbit focused on some genes with genetic and genomic sequence information including those encoding: soluble circulating immunoglobulin molecules (Igs) and their surface-bound forms on B lymphocytes (BCRs); T-cell receptors on T lymphocyte surfaces, (TCRs); the rabbit Leukocyte Antigen (RLA) complex (proteins on cells that function to present antigen fragments to TCRs); and some cytokine genes that encode key regulators of T- and B-cell responses.
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Mainolfi, Elizabeth A., Steven D. Marlin, and Robert Rothlein. "Detection and Characterization of Circulating ICAM-1." In Structure, Function, and Regulation of Molecules Involved in Leukocyte Adhesion, 367–72. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9266-8_31.

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Bravo-San Pedro, José Manuel, and Federico Pietrocola. "Autophagy assessment in circulating leukocytes." In Methods in Cell Biology. Elsevier, 2020. http://dx.doi.org/10.1016/bs.mcb.2020.10.013.

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Hofbauer, Thomas M., Anna S. Ondracek, and Irene M. Lang. "Neutrophil Extracellular Traps in Atherosclerosis and Thrombosis." In Handbook of Experimental Pharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/164_2020_409.

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AbstractDespite effective therapeutic and preventive strategies, atherosclerosis and its complications still represent a substantial health burden. Leukocytes and inflammatory mechanisms are increasingly recognized as drivers of atherosclerosis. Neutrophil granulocytes within the circulation were recently shown to undergo neutrophil extracellular trap (NET) formation, linking innate immunity with acute complications of atherosclerosis. In this chapter, we summarize mechanisms of NET formation, evidence for their involvement in atherosclerosis and thrombosis, and potential therapeutic regimens specifically targeting NET components.
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Burchiel, Scott W., and James L. Weaver. "Uses of Flow Cytometry in Preclinical Safety Pharmacology and Toxicology." In Flow Cytometry for Biotechnology. Oxford University Press, 2005. http://dx.doi.org/10.1093/oso/9780195183146.003.0020.

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During the last decade, commercial bench-top and multilaser flow cytometers have become widely available in academic, industrial, and government research laboratories. These flow cytometers provide a broad range of applications for multilaser and multiparameter analyses with user-friendly software interfaces. The purpose of this chapter is to review currently available and specialized applications of flow cytometry in preclinical pharmacology and toxicology. It is now common for most research and development, safety pharmacology, and safety assessment/toxicology groups to have direct access to flow cytometry instrumentation and technology. Many pharmaceutical companies have developed preclinical research groups that combine certain aspects of pharmacology and toxicology into early stages of drug discovery and development. The reason for this is that many new chemical entities (these are usually xenobiotics, i.e., nonindigenous chemicals) with interesting pharmacologic properties have proved to have unsuspected toxicities, but these effects are often undetected until late in development. Because drug toxicity is often not associated with the pharmacology of chemical agents, it is sometimes possible to select novel chemicals with excellent pharmacologic efficacy with minimal or reduced toxicity or potential for drug interactions. As will be discussed later in this chapter, flow cytometry has many desirable features that allow for high-throughput analysis of xenobiotics, as well as a definition of rare target cells and the measurement of biochemical endpoints. Thus, flow cytometry is finding increasing numbers of applications in preclinical pharmacology and toxicology and is being incorporated into all phases of drug discovery: development, preclinical, and clinical safety evaluation. Because of the longstanding use of flow cytometry in the evaluation of peripheral blood and hematopoietic cells in humans and other species, immunotoxicology was one of the first areas of toxicology to use flow cytometry and to develop routine testing procedures. Therefore, this chapter will largely focus on numerous applications of flow cytometry in immunotoxicity evaluation. Another factor that is driving the use of flow cytometry in immunotoxicology is that new regulations have been implemented in Europe and are being proposed in the United States and Japan to incorporate flow cytometry surface marker evaluation of circulating leukocytes in routine preclinical toxicology testing of pharmaceuticals in animals.
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Hartley, Emma L., Jonathan Millar, and John F. Fraser. "The Unholy Blood–Biomaterial Interaction in Extracorporeal Circulation." In Extracorporeal Membrane Oxygenation, edited by Marc O. Maybauer, 131–44. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197521304.003.0012.

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Extracorporeal membrane oxygenation (ECMO) results in widespread activation of the innate immune system in response to blood contact with the nonendothelialized surface. This reaction is similar to the systemic inflammatory response syndrome (SIRS) and can result in widespread inflammation and tissue damage and may affect the function and longevity of the circuit. The pathophysiology of the inflammatory and coagulative processes involving the complex interplay of the contact system and complement and leukocyte activation are reviewed here. An understanding of these events allows for a tailored approach to current and future treatment modalities, including circuit modifications, novel pharmaceuticals, and blood purification devices.
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Bauer, Moises E., Natália P. Rocha, Wilson Savino, and Antonio L. Teixeira. "Immune Mechanisms Affecting the Functioning of the Central Nervous System (CNS)." In Immunopsychiatry, 47–64. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0003.

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This chapter presents an overview of the immune mechanisms affecting the functioning of the central nervous system (CNS). The cross-talk between the immune system and the CNS is established by three independent pathways: the humoral, neural, and cellular (leukocyte) routes. Of note, increased circulating pro-inflammatory cytokines and concomitant activation of brain-resident microglia can lead to impaired cognition and depressive behavioral symptoms. The activated microglia phenotype has been associated with neuroinflammation reported in neurodegenerative and psychiatric disorders. This chapter also reviews novel physiological roles for adaptive immunity (especially T cells) during health and disease. T cells support hippocampal neurogenesis, cognition, mood, resilience to stress, and are protective against the development of psychiatric disorders.
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WISSLER, J. H., H. RENNER, U. GERLACH, and E. LOGEMANN. "Leukocytic Polypeptide Wound Hormones: Phenotype-Selective Chemorecruitment of Bone Marrow Leukocytes into Blood Circulation (Leukocytosis-Leukopenia-Leftward Shift Reactions)." In Protides of the Biological Fluids, 1167–72. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-08-031739-7.50284-6.

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Conference papers on the topic "Circulating Leukocytes"

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Marella, Saikrishna, and H. S. Udaykumar. "Computational Modeling of Human Leukocyte." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32578.

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Leukocytes (white blood cells) occupy only about 1/600th of blood by volume [1,2]. However, in view of the fact that leukocytes are larger and much stiffer than red blood cells, their presence is critical to the fluid mechanics of blood flow in the peripheral blood vessels, where the vessel diameters are comparable to those of the cells. These circulating cells must navigate through narrow micro-capillaries and recover to their undeformed spherical shape. Leukocytes act as the first line of defense in fighting disease. Leukocyte recruitment for this role involves a series of steps, including margination to vessel walls, rolling, adhesion to the endothelium, activation and locomotion and extravasation through the vessel wall to the tissue, which is afflicted by the trauma. Because the leukocyte is stiff and difficult to deform it can plug occluded micro-capillaries, leading to events such as ischemic stroke. Furthermore, leukocyte agglomeration and subsequent emolization can have serious consequences in patients under trauma, causing organ loss or even fatalities due to ischemia reperfusion injury. In these various scenarios, the rheological behavior, i.e. the physics of deformation and recovery of leukocytes under a wide variety of imposed flows, is essential.
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Subramaniam, Dhananjay Radhakrishnan, and David J. Gee. "Hydrodynamic Recruitment of Leukocytes Is Influenced by Adherent Cell Morphology." In ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-86502.

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Innate immunity depends on the coordinated activity of multiple leukocytes at or near the site of tissue injury. Previous numerical studies have shown that an adherent leukocyte can hydrodynamically recruit a free-stream leukocyte towards the endothelial surface. Using a computer model we created, we numerically investigated the hydrodynamic recruitment of circulating cells due to the presence of a nearby adherent deformed cell. For circulating cells positioned one diameter or more above the reactive surface and subsequently involved in a glancing (out-of-plane) collision with an adherent cell, the simulation indicated that the free-stream cell could be driven closer to the surface. This behavior was seen to depend, in part, on the offset glancing distance. Furthermore, for a deformed adherent cell a similar effect was observed, but beginning at smaller offset glancing distances. We also examined the binary interaction for a free-stream cell initially less than one diameter above the surface. For fixed offset glancing distances, the binary interaction with a more significantly deformed adherent cell resulted in enhanced recruiting effectiveness, as quantified by the time needed for the cell to descend to a height where receptor-ligand interactions were possible.
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Nash, Gerard B. "Studying Inflammatory Responses of Endothelial Cells and Leukocytes in Perfused Microchannels." In ASME 4th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2006. http://dx.doi.org/10.1115/icnmm2006-96013.

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Circulating leukocytes must adhere to the endothelial cells (EC) that form the lining of blood vessels, and migrate through them to carry out their protective immune functions. During inflammation this recruitment is typically controlled by cytokines released from tissue that act on the EC. The endothelial cells respond by increasing the expression of adhesion molecules on their surface (to capture flowing leukocytes), and also by presenting chemotactic agents (to induce the captured cells to migrate). This recruitment process is influenced by the local haemodynamic milieu in several ways: interactions with red cells modify the distribution of leukocytes in the blood stream; flow velocity and shear stress influence the formation and breakage of adhesive bonds; flow forces act on EC and modify their responses to inflammmatory cytokines. Microchannels have been widely used to study these processes, especially the specific receptors required for capture of isolated flowing leukocytes and their ability to support adhesion as a function of fluid shear stress. We developed a versatile system based on pre-fabricated glass capillaries with rectangular cross-section (microslides) in which we cultured EC, and which could also be coated with purified adhesion receptors for reductive studies. We also developed fluoresence-microscope-based systems for using these microslides to observe adhesion in flowing whole blood, and multiple parallel cultures for studying the effects of conditioning the EC by growth at different levels of shear stress before investigations. The microslides are available in various dimensions, and smaller versions can be used to generate high circulatory stresses when small volumes of materials (such as blood from genetically modified mice) are available. With these systems, we have for instance, been able to show how varying the concentration and aggregability of red blood cells alters leukocyte adhesion, and how expression levels of endothelial genes which underly inflammatory responses are modified by culture at a range of shear stresses mimicking different regions of the circulation.
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Jamal Jameel, Kaschin, Sarah Yanik, Eike Bülthoff, Faisal Yusuf, Birte Struck, Simon Rohde, Kai Pfeifer, et al. "Rhinovirus-induced cytokine production of circulating leukocytes is reduced in severe asthma." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.318.

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Savale, L., A. Chaouat, E. Marcos, G. Gary-Bobo, L. Boyer, B. Maitre, M. Sami, et al. "Shortened Telomeres in Circulating Leukocytes of Patients with Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3762.

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Shin, Hye-Won, Frank P. Zaldivar, Shlomit Radom-Aizik, Szu-Yun Leu, Scott Graf, and Dan M. Cooper. "Simultaneous Measurement Of No In Circulating Leukocytes (Intracellular) And Exhaled Breath Following Exercise Challenge." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5571.

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Kerstenetzky, Maria Eduarda Borges, Amanda Forte Mendes Tejo Salgado, Vitoria Ferreira David Melquiades, Vinicius Rafael Agostinho Gomes, Denise Sobral Viana, Jurema Telles de Oliveira Lima, Marcelo Ramos Tejo Salgado, and Leuridan Cavalcante Torres. "ANALYSIS OF THE LEVEL OF CIRCULATING LEUKOCYTE PLATELET AGGREGATES IN WOMEN WITH BREAST CANCER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2024.

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Objective: To evaluate the levels of circulating platelet–leukocyte aggregates in women with breast cancer (BC). Methods: A cross-sectional study was carried out between 2018 and 2019 with 27 women, who aged between 18 and 60 years, diagnosed with BC and 15 healthy women (controls). For the evaluation of the circulating platelet aggregate, samples of peripheral blood were collected at the time of routine laboratory tests for diagnosis and before treatment. Platelet aggregate analysis was performed using monoclonal antibodies by flow cytometry. Mann–Whitney U and Kruskal–Wallis tests were used to analyze medians between two and three groups, respectively. Values of p<0.05 were considered statistically significant. Analyses were performed on Graphpad v7.0. Results: In the analysis of the percentages of platelet–lymphocyte aggregates (AGP – lymphocytes) and platelet–neutrophils (AGP – neutrophils), no significant differences were observed between patients and controls. However, it was observed that the patients presented high percentage values of aggregate platelet–monocytes (AGP–monocytes) when compared with controls (p<0.0001). No significant differences were observed in the percentage levels of AGP–lymphocytes and AGP–neutrophils between the luminous subtypes A/B, HER2+, and triple-negative, and between these tumor subtypes and controls. The percentage values of AGP – monocytes were high in the luminous subtypes A/B, HER2+, and triple negative when compared with controls (p=0.008, 0.0001, 0.0002, respectively). However, no significant percentage differences in AGP–monocytes were observed between tumor subtypes. Conclusion: The present study showed the involvement of AGP–monocyte in triple-negative breast cancer and HER2+, these tumor subtypes being more aggressive and with a worse prognosis. Based on these data, the importance of new studies based on an investigation of the role of interactions between platelets and immune system cells in breast cancer became clear. The molecules involved in the linkages between platelets and leukocytes may be possible therapeutic targets.
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Williams, T. J., M. Rampart, S. Nourshargh, P. G. Hellewell, S. D. Brain, and P. J. Jose. "INTERACTION OF POLYMORPHONUCLEAR LEUKOCYTES AND ENDOTHELIAL CELLS : FUNCTIONAL CONSEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643985.

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The mechanisms involved in the accumulation of polymorphonuclear leukocytes (PMNs) in an inflammatory reaction are complex. A key phase in this process is the attachment of the PMN to the microvascular (venular in most tissues) endothelial cell, initiated by the extravascular generation of a chemical mediator. Experiments in vitro suggest that mediators, such as C5a, may act in vivo by stimulating the increased expression of the CD18 complex on the surface of the PMN within the venule lumen (1), whereas IL-1 may act by causing the expression of an adhesive molecule on the endothelial cell (2). In vitro the former process is rapid whereas the latter is slow in onset. We have measured the local accumulation of intravenously-injected Ulln-PMNs in response to intradermally-injected mediators in the rabbit, in order to investigate possible mechanisms in vivo. PMN accumulation was found to be rapid in onset in response to C5a, the rate of accumulation falling progressively to low levels by 4 hours. In contrast PMN accumulation in response to IL-1 was slow in onset, reaching a peak rate at 3-4 hours. Intradermal injection of the vasodilator prostaglandins PGI2; PGE2 and the neuropeptides VIP and CGRP caused a marked potentiation of the rate of leukocyte accumulation. PMN accumulation induced by C5a was associated with increased microvascular permeability, as indicated by the leakage of intravenously-injected 125I-albumin with a time-course in parallel with the rate of PMN accumulation enhanced by intradermally-injected vasodilators. Depletion of circulating PMNs abolishes these responses to C5a (3). In contrast, leukocyte accumulation induced by IL-1 was associated with little plasma protein leakage, even in the presence of intradermal vasodilators. This observation indicates that PMN emigration itself does not lead to increased microvascular permeability. C5a, but not IL-1, may stimulate emigrating PMNs to secrete an endogenous factor that increases permeability by an action on endothelial cells (3). This factor does not appear to be the phospholipid PAF (4). In contrast to the enhancing effects of local PGI2, intravenously-infused PGI2 inhibited PMN accumulation induced by C5a and IL-1, and plasma protein leakage induced by C5a (5). This effect is probably mediated by elevation of cyclic AMP in intravascular PMNs. We have shown that C5a stimulation of PMNs in contact with endothelial cells in vitro induces endothelial cell PGI2 secretion (6). Thus, PGI2 may be part of a negative feedback system in vivo to control interactions between PMNs and endothelial cells.These observations provide some clues to the intricacies of mechanisms of leukocyte accumulation in vivo.
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Schatz, Tim, Abby Beltrame, Sarah Howard, and Mark Smith. "Modification of the ASTM Platelet and Leukocyte Assay: Use of an Alternative and Clinically Relevant Anticoagulant — An In-Vitro Hemocompatibility Assessment of Blood Contacting Medical Devices." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3345.

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The purpose of this test method is to assist in the determination of the thrombogenic potential of medical materials exposed to human whole blood. By evaluating surface-induced activation, platelet adherence to a material, and platelet and leukocyte depletion from blood, a material’s potential for thrombus formation can be assessed. If a significant decrease in platelets and/or leukocytes is observed in whole blood when compared to a blank control, the tested material has the potential to induce an in-vivo thrombogenic response. The present standard for the testing of platelet and leukocyte response to cardiovascular materials, ASTM F2888-13, Standard Test Method for Platelet Leukocyte Count - An In-Vitro Measure for Hemocompatibility Assessment of Cardiovascular Materials [1], mandates the use of several reference materials in the presence of blood anticoagulated with sodium citrate. This study was designed to address the relevance of the assay method when using a potent anticoagulant, 3.2% sodium citrate, to evaluate the thrombogenic potential of medical devices. Current studies on this question are under investigation at the FDA also with the intent of improving the standard methods for this assay by evaluating blood anticoagulated with 2–3 IU/mL of heparin [2]. For this study, the effects of several biomaterials were evaluated when exposed to blood anticoagulated with sodium citrate and, concurrently, an even lower dose of heparin at 1 IU/mL also used by our laboratory in a new circulating in vitro assay for thrombogenicity [3]. We believe this test method allows for a sensitive assay that can more accurately predict potential thrombogenic outcomes of cardiovascular materials, while maintaining appropriate responses in both positive and negative control materials.
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Kloetgen, Andreas, Jonathan Serrano, Seema Patel, Christopher Bowman, Guomiao Shen, David Zagzag, Matthias A. Karajannis, et al. "Abstract 3658: DNA methylation of circulating tumor educated leukocytes predicts IDH1/2 mutation status in adult patients with diffuse gliomas." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3658.

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